2009 article on how scientist changed one gene to change sex of mouse

http://www.geneticsandsociety.org/article.php?id=5011

Simple gene technique changes sex of a mouse From Minnie to Mickey (and all they did was turn off a gene) by Steve Connor, The Independent December 11th, 2009

The battle of the sexes is a never-ending war waged within ourselves as male and female elements of our own bodies continually fight each other for supremacy. This is the astonishing implication of a pioneering study showing that it is possible to flick a genetic switch that turns female ovary cells into male testicular tissue. For decades, the battle of the sexes has been accepted by biologists as a real phenomenon with males and females competing against each other - when their interests do not coincide - for the continued survival of their genes in the next generation. Now scientists have been able to show that a gender war is constantly raging between the genes and cells of one individual. One of the great dogmas of biology is that gender is fixed from birth, determined by the inheritance of certain genes on the X and Y sex chromosomes. But this simplistic idea has been exploded by the latest study, which demonstrated that fully-developed adult females can undergo a partial sex change following a genetic modification to a single gene. The findings suggest that being male or female is not a permanently fixed state but something that has to be continually maintained in the adult body by the constant interaction of genes to keep the status quo - and the gender war - from slipping in favour of the opposite sex. The results could explain some of the great mysteries of human gender, for instance why some women after the menopause develop male characteristics, such as facial hair and deeper voices, or why other people are so unhappy with the gender they were born with that they seek hormone therapy and radical sex-change operations. Scientists said that the study also contradicted another biological dogma - that the "default" gender is female, with all embryos starting out as female unless they possess a male sex-determining gene. Although this remains true in terms of how gender is determined in the womb, the latest findings show that it is still possible to convert an adult female's ovaries into testosterone-producing testes. The study was carried out on mice but the implications are relevant to humans, the scientists said. By switching off a gene called FoxL2, which exists in all mammals, the ovary cells of adult female mice developed spontaneously into the fully developed, testosterone-producing cells found in male testes, although they could not produce sperm. "We take it for granted that we maintain the sex we are born with, including whether we have testes or ovaries," said Robin Lovell-Badge, from the Medical Research Council's National Institute of Medical Research in north London, who was part of the international team led by the European Molecular Biology Laboratory in Heidelberg. "But this work shows that the activity of a single gene, FoxL2, is all that prevents adult ovary cells turning into cells found in testes. If it is possible to make these changes in adult humans, it may eventually remove the need for surgery in gender-reassignment treatment," Dr Lovell-Badge said. "If this does become possible, it's likely that while treated individuals would make the right hormones for their new sex, fertility would be lost. It's still very speculative, but it's possible that this approach could produce an alternative to surgery and the removal of gonads - ovaries and testes. It's a little more natural, but of course anyone undergoing such a sex change would be infertile," he added. The study, published in the journal Cell, found that the female-promoting FoxL2 gene works by suppressing a male-promoting gene called Sox9. In the adult female mice where FoxL2 was artificially switched off, the Sox9 quickly took over, sending chemical signals that converted the ovary's female cells into the testosterone-producing cells normally found only in the testes. The female mice produced levels of testosterone normally found in male mice - 100 times higher than the concentrations found in ordinary female mice. This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of biotechnology and public policy issues. We believe this constitutes a 'fair use' of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes. For more information go to: http://www.copyright.gov/title17/92chap1.html#107. If you wish to use copyrighted material from this site for purposes of your own that go beyond 'fair use', you must obtain permission from the copyright owner.

Research article on comparison of trans woman to female brain

I am in the process of setting up another blog with just research on gender, hormones but I wanted to share this article for now with everyone

Thank you ,
Rachel

http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564

Results

Section:

- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Results

Section:

- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Results

Section:

- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).

- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

Differences among the groups were statistically significant by the nonparametric Kruskal-Wallis multiple comparison test (P = 0.002 for SOM neuron number). No statistical group differences were found for age (P = 0.090), brain weight (P = 0.125), postmortem time (P= 0.738), fixation time (P = 0.065), or storage time (P = 0.308). To further test whether the differences in the BSTc between the groups were affected by possible confounding factors, such as paraffin-embedded storage time of sections, fixation time, postmortem time, or brain weight, an analysis of covariance was carried out. These factors seemed to have no significant effect on the BSTc SOM neuron numbers (P > 0.10).
The number of SOM neurons in the BSTc of heterosexual men (32.9 ± 3.0 × 10³) was 71% higher than that in heterosexual women (19.2 ± 2.5 × 10³) (P < 0.006), whereas the number of neurons in heterosexual and homosexual men (34.6 ± 3.4 × 10³) was similar (P = 0.83). The BSTc number of neurons was 81% higher in homosexual men than in heterosexual women (P < 0.004). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of females (19.6 ± 3.3 × 10³) (P = 0.83) (see also Figs. 1 and 2). In addition, the neuron number of the FMT was clearly in the male range (see Fig. 1). The number of neurons in transsexuals was 40% lower than that found in the heterosexual reference males (P < 0.04; see the legend to Fig. 1) and 44% lower than that found in the homosexual males (P < 0.02). Including patients S2, S3, and S5 in the male group and S1, S6, and M2 in the female group or S7 in the transsexual group to increase the number of their respective gender groups enhanced the level of significance among the groups (P < 0.001 for SOM neuron number). There seemed to be no clear difference in the BSTc number of neurons between early onset (T2, T5, T6) and late-onset transsexuals (T1, T3), indicating that their smaller number of neurons is related to the gender identity per se rather than to the age at which it became apparent. No indication was found for a relationship between cause of death and BSTc neuron numbers. Analysis of the BSTc volumes showed a similar pattern of differences among the groups with heterosexual men having a BSTc volume of 4.60 ± 0.28 mm³, similar to that in homosexual men (5.00 ± 0.39 mm³) (P = 0.76). The BSTc volume of females (3.38 ± 0.41 mm³) and that of transsexuals (3.58 ± 0.19 mm³) did not differ either (P = 0.50). The volumes of all males, regardless of sexual orientation, vs. all females or vs. all genetic male transsexuals were statistically highly significant (P ≤ 0.01). The FMT had a BSTc volume in the male range (4.80 mm³).
- See more at: http://press.endocrine.org/doi/full/10.1210/jcem.85.5.6564#sthash.5OKpfRtK.dpuf

copy and paste of a discussion on trans people in the Oymplics ....... why we hide ?

people seem to not understand the hostility on both sides of the fence. it is not pretty on this side of the fence but when a trans person, can be one, lashes out at others it  makes all of us look bad!! should not be this way, but it was like this as a Marine in the lase 70's too.  but to down play what is done to many of us is very hurtful, the plight of the trans comm against women; are you serious dude? the facts are otherwise, 603 dead in 7 yrs in brazil. we are killed and it simply does not make the news!!! the trans girl found dead in a field in texas, the list goes on and on....

Rachel Reid after 4 yrs of HRT , and one that served 2 tours in the Marines, the amount of muscle mass lass after 2 yrs was massive , my testosterone is ...7 and as been lower and the norm for a woman is .1-.8. not to mention my estradiol level is now 149 so this thought that someone like me would have a muscular advantage is seriously flawed. i talked to another trans woman marine and she has the same issue with muscle mass loss. there is no advantange if on HRT.

Like · Reply · 23 · January 22 at 9:20am

Jessie  Except when sexual dimorphism comes into play (ie height and bones)

Like · Reply · 4 · January 22 at 9:34am

Shannon Humans don't even have much sexual dimorphism. There are plenty of women taller and stronger than men. It's not a valid argument to exclude trans women. There is NO valid argument to exclude trans people in general.

Rachel Reid i lost one inch in height, now at 5'6" and the estrogen allow the hips to shift forward in the tendons..... there is no advantage .... it is an equal playing field..... i benched at 20 yo 240 lbs in the Marines, at 51 yo when i started HRT i could do ...See More

Like · Reply · 6 · January 22 at 10:39am

Jessica It's a lot... I have recently stopped field work because I just can't do it anymore. With the hormones on top of my old injuries I can't perform like I used to. The changes are immense... You can't understand without going through them but you can take or word.

Hemming  I know a fair few cis women taller and stronger than some cis dudes I know

Sid  Rachel Reid Thank you for your service smile emoticon ( in the marines )

Rachel Reid Sid Menon uw and thank for that compliment too

Like · Reply · 2 · January 22 at 4:02pm

Lisa Rosenfield Right. Just walking down the street I can hardly tell a male from a female. Women are just as hairy, men's hips are wide, women's voices are just as deep. And as a massage therapist I can hardly tell the difference when I touch bodies. I have to be really careful not expose men's breasts. Yes, sarcasm intended.

Like · Reply · 1 · Yesterday at 8:14am

Jacqui Broekhof oh ffs

Like · Reply · Yesterday at 1:29pm

Jacqui Broekhof you have to be joking Lisa Rosenfield! you cant tell a male from a female? i do bodywork and the difference is immediately obvious. Who are you trying to kid?

Like · Reply · Yesterday at 1:31pm

Jacqui Broekhof Rachel Reid you are deluded

Like · Reply · Yesterday at 1:33pm

Kelsey Jay Bullshit--- you don't all the sudden have the strength of a woman just because you take estrogen.

Unlike · Reply · 1 · Yesterday at 1:52pm

Tori Barron Thank you Dr. Jay...

Like · Reply · 1 · Yesterday at 1:57pm · Edited

Kelsey Jay Btw--- why so many Transgender males in the armed forces??? What exactly do they do to you guys??

Like · Reply · Yesterday at 2:23pm

Rachel Reid I hear it is because we prove to be a man..... but i think it more simplistic ...... with me i lived in a small town , Hollidaysburg, pa, population maybe 10k, and the one way of thinking and no options, left me few options since my family was not rich...See More

Like · Reply · Yesterday at 2:48pm · Edited

Kelsey Jay Just because you liked feminine things and had feminine behaviors does not make you a girl... your biology doesn't change just because you like girly things...

Like · Reply · 23 hrs

Rachel Reid first you do not know me and i cannot argue with people that think the world is flat. but the fact is the largest sex organ in the body is the brain not what is between your legs and I will leave it at that !!!

Like · Reply · 23 hrs

Kelsey Jay Sorry, women don't have dicks...

Like · Reply · 1 · 21 hrs

Rachel Reid your lack of intelligence is noted and some women do not have uterus, one woman posted today that she had a MRI which showed some male parts which explain the need for HRT , yet she has a uterus and is pregnant........ you are crude, rude and hurtful but also wrong! you and others like you are the reason only a few of us come out to speak about our lives .... it is sad

Like · Reply · 1 · 20 hrs · Edited

Rachel Reid i just read your page of how you share your views and you were threatened by rape and murder by the trans comm.... i am deeply sorry others have resorted to such low tactics and threats against you.. i am can assure you that not all of us are like the ...See More

Like · Reply · 1 · 20 hrs

Frank Sumner Rachel, you still have the build of a man. I have women friends who are as tall as me, who work out and play sports, who even though they work out more than I do, I can put them in a hold real quick. I am a man and that means something, right? My si...See More

Like · Reply · 1 · 4 hrs · Edited

Rachel Reid has nothing to do with a woman.......... people need to research and the science is behind me, us, no i have the muscle mass of a woman, the brain too the white and gray matter is the same as female not male please look at the research before making co...See More

Like · Reply · 2 hrs

Rachel Reid like a mutation in other species exist , which is male body and female qualities , but it cannot happen in humans....that is totally absurd....nothing is black and white ...... there is plenty of gray

Like · Reply · 2 hrs

Rachel Reid also the estrogen , which happened when i was teen, shifted forward due to estrogen.... this is scientific fact ....google estrogen and hips shifting forward.......

Like · Reply · 2 hrs

Frank Sumner Women are BUILT differently, you do know that?

Like · Reply · 1 · 2 hrs

Rachel Reid look at the research .... it says otherwise .... it all depends on family DNA and genes with many transgender id people they might need from 100-400 mg of Spiro to block testosterone, and people like me need zero. there is not a black and white answer...See More

Like · Reply · 2 hrs · Edited

Rachel Reid here is an article of how hormones affect injuries in women....... it is hormone based ...... take a peek........http://ajs.sagepub.com/content/30/2/182.abstract

The Effect of the Menstrual Cycle on Anterior Cruciate Ligament…

ajs.sagepub.com

Like · Reply · Remove Preview · 2 hrs

Rachel Reid here is prospective on me vs male!! i am sure most men can maintain an erection however with me baring massive doses of Viagra and divine intervention i will never have one again. plus i have 3 non cancerous cyst in my left breast so i need mammograms each yr . no one chooses this ...... trust me

Like · Reply · 1 min